首例耐药沙门氏菌斯坦利ST29继发于急性胆囊炎。

IF 2.9 3区 医学 Q2 INFECTIOUS DISEASES
Infection and Drug Resistance Pub Date : 2025-05-05 eCollection Date: 2025-01-01 DOI:10.2147/IDR.S507875
Wenqing Wang, Shufen Liu, Minlan Zhang, Yan Chen, Yanru Liang, Shuqi You, Peijun Lv, Xuebin Xu, Fenghua Zhang
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引用次数: 0

摘要

目的:分析从急性胆囊炎继发慢性腹泻患者中分离出的一株非伤寒性胆汁沙门氏菌的表型和基因组特征。方法:患者以急性胆囊炎继发慢性腹泻2周。非伤寒沙门氏菌胆汁分离物通过生化试验、质谱、血清凝集试验和抗微生物药敏试验进行鉴定。随后,采用全基因组测序(WGS)对分离物的血清型、多位点序列分型(MLST)、耐药基因(AMR)、移动遗传元件(MGEs)和毒力基因进行预测和注释。结果:经生化检验和质谱分析,分离物为沙门氏菌。经血清凝集试验鉴定的分离物血清型与WGS预测一致,鉴定为Stanley沙门氏菌(1,4,5,12:d:1,2, ST29)。对氨苄西林、环丙沙星、头孢噻肟、阿奇霉素、甲氧苄啶/磺胺甲恶唑、氯霉素等6种抗菌剂耐药。共筛选到5大类抗菌药物14个耐药基因,其中β-内酰胺耐药基因为:bla TEM-1B、bla OXA-1、bla DHA-1;喹诺酮类耐药基因:qnrB4和aac(6′)-Ib-cr;大环内酯类耐药基因:mph(A)、mph(E)和msr(E),叶酸途径抑制剂耐药基因:sul1、sul2和dfrA14;氯霉素耐药基因:floR、catA2、catB3。在喹诺酮耐药决定区(QRDR)检测到parC基因T57S突变。预测3个质粒复制子(IncHI2/IncHI2A、IncR、IncN)和3个插入MGEs。共预测到42个毒力基因,其中25个为分泌和转运基因,10个为菌毛粘附基因。在沙门氏菌致病性岛1号(SPI-1)中仅发现1个侵袭性蛋白调控基因(inv),未发现伤寒毒素基因。结论:从一例胆囊炎继发腹泻患者中分离到的斯坦利沙门氏菌ST29具有高耐药性和相对低毒力的特点。这突出了在临床实践中需要提高对侵袭性病例的警惕,以及与耐抗生素沙门氏菌分离菌肠道迁移相关的重大疾病负担。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
The First Case of Antimicrobial-Resistant Salmonella Stanley ST29 Diagnosed Secondary to Acute Cholecystitis.

Objective: To analyze the phenotypic and genomic characteristics of a non-typhoidal Salmonella bile isolate from a patient with chronic diarrhoea secondary to acute cholecystitis.

Methods: The patient presented with chronic diarrhoea lasting for two weeks, which was secondary to acute cholecystitis. The non-typhoidal Salmonella bile isolate was identified using biochemical tests, mass spectrometry, serum agglutination tests, and antimicrobial susceptibility testing. Subsequently, whole-genome sequencing (WGS) was performed to predict and annotate the serotype, multilocus sequence typing (MLST), antimicrobial resistance genes (AMR), mobile genetic elements (MGEs), and virulence genes of the isolate.

Results: The isolate was identified as Salmonella spp. by biochemical tests and mass spectrometry. The serotype of the isolate identified by serum agglutination tests was consistent with WGS prediction and was identified as Salmonella Stanley (1,4,5,12: d:1,2, ST29). It was resistant to six antimicrobial agents, including ampicillin, ciprofloxacin, cefotaxime, azithromycin, trimethoprim/sulfamethoxazole, and chloramphenicol. Five major classes of antimicrobial agents, comprising a total of 14 resistance genes were screened, including β-lactam resistance genes: bla TEM-1B, bla OXA-1, and bla DHA-1; quinolone resistance gene: qnrB4 and aac(6')-Ib-cr; macrolide resistance genes: mph(A), mph(E), and msr(E), and folate pathway inhibitor resistance genes: sul1, sul2, and dfrA14; chloramphenicol resistance genes: floR, catA2 and catB3. T57S mutation in the parC gene was detected in the quinolone resistance-determining region (QRDR). Three plasmid replicons (IncHI2/IncHI2A, IncR, IncN) and three insertion MGEs were predicted. Forty-two virulence genes were predicted, of which 25 were secretion and transporter genes, and ten were fimbrial adherence genes. Only one invasive protein-regulated gene(inv) was found in Salmonella Pathogenicity Islands 1(SPI-1), and no Typhoid toxin genes were predicted.

Conclusion: The case of Salmonella Stanley ST29 isolated from a patient with diarrhoea lasting 55 days secondary to cholecystitis aligns with the characteristics of high drug resistance and relatively low virulence. This highlights the need for increased vigilance in clinical practice regarding invasive cases and the significant disease burden associated with the intestinal migration of antimicrobial-resistant Salmonella isolates.

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来源期刊
Infection and Drug Resistance
Infection and Drug Resistance Medicine-Pharmacology (medical)
CiteScore
5.60
自引率
7.70%
发文量
826
审稿时长
16 weeks
期刊介绍: About Journal Editors Peer Reviewers Articles Article Publishing Charges Aims and Scope Call For Papers ISSN: 1178-6973 Editor-in-Chief: Professor Suresh Antony An international, peer-reviewed, open access journal that focuses on the optimal treatment of infection (bacterial, fungal and viral) and the development and institution of preventative strategies to minimize the development and spread of resistance.
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